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Background: Cervical cancer survivors tend to have specific risk factors for developing cancers of other sites later in life: infection with the human papillomavirus (HPV), history of smoking, and/or treatment with radiation therapy. The recent licensure of HPV vaccines will likely decrease the development of primary in situ and invasive cervical and possibly other HPV-related cancers. Since the HPV vaccine has the ability to impact more than one HPV-related cancer in the same individual, we examined the risk in developing subsequent primary cancers (in situ and invasive) among cervical cancer survivors.
 Methods: Using the Surveillance Epidemiology and End Results (SEER) 13 Cancer Registry data (1992-2004), 23,509 cervical cancer survivors were identified and followed up for a mean of 4.75 person-years for the development of subsequent primary cancers. Index cases where cervical cancer was not the first diagnosed cancer were excluded. Also, index cases were stratified by mode of treatment (radiotherapy). Subsequent HPV-associated cancers (vaginal, vulvar, anal, rectal, and oropharyngeal) were considered if they were diagnosed 2 or more months after initial diagnosis of the first cancer. Observed number (O) of subsequent cancers were compared with those expected (E) based on age-/race-/year-/site-specific rates in the SEER population. The standardized incidence ratio(SIR) represents 'O / E'. All reported SIRs were considered statistically significant if they differed from 1, with an alpha level of 0.05.
 Results: We identified 1088 subsequent primary cancers (in situ=186, invasive=902). There is a significant elevated risk for subsequent in situ cancers of the vagina and the vulva (SIRs = 53.82, 6.58 respectively). Also, there is significant elevated risk for invasive vaginal, vulvar, and rectal cancers (SIRs = 29.9, 5.7, and 2.2 respectively). Elevated risk was observed for invasive cancer of oral cavity and pharynx (SIR=1.68); however, it was not statistically significant. Significant elevated risk for subsequent invasive cancers of vagina was observed among those who had and did not have radiotherapy for treatment (SIRs = 29.66, and 30.38 respectively). Also, significant elevated risk for subsequent vaginal in situ (SIRs for White=49.4, Black=52.8 and Asian Pacific Islander=91.4) and invasive cancers (SIRs for White=25.7, Black=34.5 and Asian Pacific Islander=48.5) was observed by race.
 Conclusions: Using a population-based cancer registry, we observed increased risk in development of subsequent HPV-associated in situ and invasive cancers among cervical cancer survivors. These risks are independent of radiotherapy. The results have implications for the development of prevention strategies among cervical cancer survivors as the role of HPV becomes evident in development of subsequent primary in situ and invasive cancers.


99th AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA